Summary of Study ST000417

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000326. The data can be accessed directly via it's Project DOI: 10.21228/M8C31Q This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST000417
Study TitleControlled Human Exposure to Particulate Matter (PM) and Gaseous Co-Pollutants
Study TypeExposome Evaluation
Study SummaryThis study is designed to provide the environmental aspects to support both the acquisition of study samples and the advancement of environmental chemical speciation information and data analyis needed. The aims of the study are as follows:1)Do the metabolomics profiles appear to be impacted by exposure to PM and NO2+PM. 2)are the metabolomic profiles related to the PM and NO2+PM distinct 3)which features (chemical or physical) of the PM and NO2+PM have the most significant impact on the metabolomic profiles.
Institute
RTI International
DepartmentRCMRC
Last NameSumner
First NameSusan
Address3040 E Cornwallis Road, Research Triangle Park, NC, 27519, USA
Emailssumner@rti.org
Phone919-541-7479
Submit Date2016-06-15
Num Groups3
Total Subjects87
Num Males47
Num Females40
Raw Data AvailableYes
Raw Data File Type(s)cdf
Analysis Type DetailGC-MS
Release Date2018-06-05
Release Version1
Susan Sumner Susan Sumner
https://dx.doi.org/10.21228/M8C31Q
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000326
Project DOI:doi: 10.21228/M8C31Q
Project Title:Controlled Human Exposure to Particulate matter (PM) and Gaseous Co-Pollutants
Project Type:Exposome Evaluation
Project Summary:During the past decade, several epidemiological studies have reported statistically significant positive correlations between daily concentrations of ambient air particles and acutely increased mortality and morbidity. It has been estimated that 50,000 - 60,000 excess deaths in the U.S. each year may be attributable to ambient particles. Several panel studies have reported associations between fine PM and decreased heart rate variability and increased vascular markers of inflammation. In addition, recent controlled human exposure studies have reported that fine particles can increase pulmonary inflammation, decrease heart rate variability, and increase vascular factors of inflammation and blood coagulation. However, these latter studies only assessed the effects of particulate matter. In the real world, people are simultaneously exposed to both gaseous pollutants (e.g. ozone, nitrogen dioxide) and particles. Recognition of this leads the National Research Council to list studies of PM and gaseous co-pollutants as one of the ten highest priorities in PM research. One of these co-pollutants that frequently occur together with PM is nitrogen oxides (NOx), which is produced during combustion processes. NOx consists of nitric oxide (NO) and nitrogen dioxide (NO2). NO dominates near roadsides and peaks in morning rush hours while NO2 levels show less temporal and spatial variability. NO and NO2 concentrations may reach values over 1 ppm and 0.5 ppm respectively during smog situations. NO2 is an oxidant capable of oxidizing and nitrating lipids and proteins and can cause cytotoxic effects on the cell membranes of epithelial cells as well as macrophages. Controlled exposure of healthy humans to 2 ppm NO2 reduced phagocytic capacity in macrophages. At similar concentrations controlled NO2 exposure produced small changes in large airway function and increased airway reactivity to methacholine. The inflammatory effects of NO2 may thus enhance the adverse effects of PM. In this study we hypothesize that NO2 and PM2.5 affect the cardiopulmonary system beyond what either pollutant is capable of inducing by itself. Cardiopulmonay impairment will be assessed by measuring changes in bronchoalveolar lavage (BAL) neutrophils and cytokines, heart rate variability, and plasma factors involved in inflammation and coagulation.
Institute:EPA
Laboratory:National Health and Environmental Effects Research Laboratory
Last Name:Devlin
First Name:Robert
Address:109 Alexander Drive, Research Triangle Park, NC 27709
Email:devlin.robert@epa.gov
Phone:919-966-6255
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